Figure 1
Schematic representation of the proposed mechanisms underlying protection from disease progression to vascular complications in patients with long-standing T1D. Higher insulin sensitivity and lower glucose levels (measured with HbA1c), and also lower accumulation of fat in the liver characterize patients with long-term T1D who never progress to vascular complications (NPs). In the liver cell, glycolytic intermediates are actively shunted into the pentose-phosphate pathway (PPP) as indicated by reduced essential cofactor thiamine, increased phenylalanine and reduced erythritol. Generated NADPH is used in reductive biosynthesis of glutathione and detoxification processes to maintain antioxidant capacity. Ribose-5-phosphate (R5P) generated in PPP, and serine, glycine and pyruvate generated in glycolysis are used in the one carbon metabolism and nucleotide biosynthesis to improve restorative capacity. Metabolism of essential amino acid tryptophan generates protective picolinic acid. Elevated factors are in red, reduced are in blue (Created with BioRender.com).
